Postharvest biocontrol ability and antagonistic mechanism of Streptomyces djakartensis MEPS155 against Ceratocystis fimbriata in sweetpotato

Sweetpotato ( Ipomoea batatas (L.) Lam.) is threatened by black rot disease caused by the fungus Ceratocystis fimbriata during both growth and postharvest stages. Streptomyces species found in the rhizosphere soil of plants are promising biocontrol agents capable of inhibiting plant pathogens through diverse mechanisms. In this study, Streptomyces djakartensis strain MEPS155 was shown to reduce the biomass of C. fimbriata , inhibit spore germination, compromise its cell wall and membrane integrity, disrupt mitochondrial function, and lower the pathogenicity. Additionally, transcriptomic analysis of C. fimbriata treated with strain MEPS155 revealed significant down-regulation of genes related to pathogenicity, cellular composition, and energy production, particularly within the mitogen-activated protein kinase (MAPK) signaling pathway, steroid biosynthesis and tricarboxylic acid cycle pathways, aligning with the phenotypic findings. The significantly down-regulated gene CfsteA (PHH54671) in the MAPK pathway was knockout through genetic transformation to obtain the mutants ( ΔCfsteA ). The mutants ΔCfsteA exhibited altered biomass, decreased conidial number and germination, damaged cell wall integrity, and reduced pathogenicity. These findings indicated that CfsteA was an important target gene for preventing and controlling sweetpotato black rot. This study provided potential strategies for managing sweetpotato black rot and inspired new insights into the pathogenic mechanisms of C. fimbriata . • MEPS155 disrupted the cell wall and membrane structure, and mitochondrial function of Ceratocystis fimbriata . • MEPS155 inhibited spore germination and virulence of C. fimbriata . • MEPS155 altered the expression of growth, oxidative stress and pathogenicity-related genes in C. fimbriata . • CfsteA deletion reduced the virulence of C. fimbriata in sweetpotato.